ArticleProgress in orthodontics2025
A novel PTH1R mutation causes primary failure of eruption via the cAMP-PI3K/AKT pathway.
Article in Progress in orthodontics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Loss of PTH 1 receptor signaling in periodontal cells drives cementum dysfunction and molar ankylosis in mice.Bone research · 2026Article
- Integrated Genetic Networks and Epigenetic Regulation inTooth Development and Maturation.Cells · 2026Review
- Genetic Determinants of Primary Failure of Eruption: A Comprehensive Review of PTH1R Variants.Genes · 2026Review
- Parathyroid hormone-related protein is a therapeutic target in idiopathic pulmonary fibrosis.Signal transduction and targeted therapy · 2026Article
- An injectable phosphocreatine-grafted hydrogel incorporating hierarchically structured teriparatide/SrZnP-functionalized Zn-Cu particles for osteogenesis-angiogenesis coupling and osteoporotic bone regeneration.Materials today. Bio · 2025Article
- Mechanisms of primary failure of eruption: a new model of multidimensional framework.Progress in orthodontics · 2025Review
- Aberrant ALPP Expression Serves as a Prognostic Biomarker and Facilitates Cholangiocarcinoma Progression through Immune Evasion and PI3K-Akt Signaling Activation.International journal of medical sciences · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
backgroundPrimary failure of eruption (PFE) is a rare disorder characterized by a posterior open bite. While mutations in the parathyroid hormone 1 receptor (PTH1R) gene have been demonstrated to cause PFE, the underlying mechanisms remain largely unknown.
methodsWhole exome sequencing was conducted to identify PTH1R variants in a PFE family. MG63 cells that stably expressed the corresponding mutant PTH1R were established using lentiviruses. Next, osteogenesis was assessed by measuring cell alkaline phosphatase activity, conducting alizarin red staining, and evaluating osteoblast-specific gene expression. Then, computational analysis of binding affinity and RNA sequencing were carried out. Lastly, rescue experiments were performed to validate the mechanism underlying the pathogenesis of PFE.
resultsA novel PTH1R missense mutation (c.904G > A, p.E302K) was identified in a Chinese family affected by PFE. Moreover, the E302K mutation inhibited the expression of osteogenic-specific genes and proteins in MG63 cells. Computational analysis revealed the E302K mutation decreased the binding affinity of Gα
conclusionsThis study indicated that the E302K mutation in PTH1R decreased the binding affinity of PTH1R protein for Gα
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